A checkpoint molecule that functions to control the expansion of allergy-inducing cells may be used as a target to develop drugs for asthma, eczema.

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An early initiator of the allergic inflammation known as a 'type 2 innate lymphoid cell' (ILC2) express a checkpoint molecule, known as'PD-L1', that functions to control the expansion of allergy.
Allergic conditions, such as asthma or eczema, arise when the immune system misfires and sparks an uncontrolled response to common allergens, such as house dust mites.
In asthma this aberrant immune response leads to immune cells infiltrating the lungs, where they cause inflammation that affects lung function and leads to difficulties in breathing.
One key cell that is an early initiator of this allergic inflammation is known as a 'type 2 innate lymphoid cell' (ILC2). These cells instruct others, known as 'Th2 cells', to drive the cascade of inflammation in the lungs that leads to the development of asthma.
In this study, using a mouse transgenic approach, the scientists demonstrated that ILC2s express a checkpoint molecule, known as'PD-L1', that functions to control the expansion of allergy-inducing Th2 cells and the development of allergic pulmonary and gut tissue inflammation.
First author of the paper, Dr Christian Schwartz, a European Molecular Biology Organization Long Term Fellow in Professor Fallon's group, added: "It is fascinating that a small cell population such as the ILC2s can regulate the expansion of Th2 cells and thereby shape the whole outcome of an immune response - be it beneficial in case of parasitic infections, or detrimental as in the case of allergic responses."
Source-Eurekalert
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